The article by Churg and Strauss discusses the relationship between allergic states and vascular lesions, particularly periarteritis nodosa. Over the past 25 years, studies have established a connection between severe asthma and vascular lesions, leading to the identification of a clinical syndrome characterized by severe asthma, fever, and hypereosinophilia, along with symptoms of vascular involvement in various organ systems. The authors present 13 cases of this syndrome, which exhibited characteristic anatomical changes, including widespread vascular lesions similar to those seen in periarteritis nodosa, and distinctive tissue alterations in the vessel walls and extravascular collagen systems. These alterations include necrosis of eosinophilic exudate, severe "fibrinoid" collagen change, and granulomatous proliferation of epithelioid and giant cells. The authors suggest that this syndrome, which they term "allergic granulomatosis," is distinct from classical periarteritis nodosa, as it is associated with allergic etiology and more severe clinical outcomes. The presence of granulomatous lesions in both vessel walls and connective tissue throughout the body supports this distinction. The article also highlights the diagnostic value of cutaneous and subcutaneous nodules for identifying allergic granulomatosis.The article by Churg and Strauss discusses the relationship between allergic states and vascular lesions, particularly periarteritis nodosa. Over the past 25 years, studies have established a connection between severe asthma and vascular lesions, leading to the identification of a clinical syndrome characterized by severe asthma, fever, and hypereosinophilia, along with symptoms of vascular involvement in various organ systems. The authors present 13 cases of this syndrome, which exhibited characteristic anatomical changes, including widespread vascular lesions similar to those seen in periarteritis nodosa, and distinctive tissue alterations in the vessel walls and extravascular collagen systems. These alterations include necrosis of eosinophilic exudate, severe "fibrinoid" collagen change, and granulomatous proliferation of epithelioid and giant cells. The authors suggest that this syndrome, which they term "allergic granulomatosis," is distinct from classical periarteritis nodosa, as it is associated with allergic etiology and more severe clinical outcomes. The presence of granulomatous lesions in both vessel walls and connective tissue throughout the body supports this distinction. The article also highlights the diagnostic value of cutaneous and subcutaneous nodules for identifying allergic granulomatosis.